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Weathering rind retains the greatest extent of the mineralogical and chemical composition information of the original mineral. Recently, we found some brownish-yellow or khaki serpentine jade weathering rinds with a thickness of 0.2–0.6 cm in Ji’an. The purpose of this paper is to explore differences in structural characteristics and chemical composition between weathering rinds and unweathered cores and summarize the formation of weathering rinds. In terms of structural characteristics, weathering rinds have smaller a0, b0, β values than unweathered cores; the specific surface area is 13.3987 m2/g; the pore volume is 0.0314 cm3/g; and the pore size distribution is characterized as more mesoporous (2–10 nm). The weathering rind shows partial dissolution of serpentine grains, increased porosity, and loosening structure. In terms of chemical composition, the weathering rind is characterized by the decrease of some serpentine major elements (Si, Mg, and Fe) and the increase of some impurity elements (Al, Ca, K, Na, and Cl). The weathering rind is the result of further alteration of serpentine jade, accompanied by the reduction of the Fe3+/Fe2+ ratio and the generation of the clay mineral (chlorite). In addition, it was also found that Ji’an serpentine jade belongs to Mg-bearing carbonate rock genesis, which are derived from marine deposits.

Background Secretory phospholipase A 2 group IIA (sPLA 2 -IIA) appears to be an important inflammatory mediator of cardiovascular disease and may play a pivotal role in the pathophysiology of AS. To understand whether the influence of sPLA 2 -IIA on proinflammantory effects in vascular endothelial cells may help comprehend the mechanism induced by the sPLA 2 -IIA involved in AS. Objectives To investigate the effect of different concentrations of sPLA 2 -IIA on Endothelial Cells, and to investigate the signalling pathway. Methods (1) HUVEC were cultured in three different concentrations groups (0.01, 0.1, 1 ug/ml) of sPLA 2 -IIA. Endothelial cell nitric oxide concentration in the supernatant was detected by kit. The mRNA expression levels of ET-1, eNOS, ICAM-1, VCAM-1 were determined by Real Time-PCR. The protein expression level were measured by Western Blot or by ELISA. (2) HUVEC cells were cultured with 1 ug/ml sPLA 2 -IIA and 10 nmol/l 4-BPB (Hydrolysis inhibitor) or 1 umol/l PD98059 (ERK1/2 inhibitor) or SP600125 (JNK inhibitor) or SB203580 (p38 inhibitor) or Bay11-7085 (NF-kB inhibitor) alone or combined. Parameters described in Method step 1 were measured. Results (1) sPLA 2 -IIA increased the mRNA and protein expression of ICAM-1, VCAM-1 and ET-1 and decreased the level of NO in a concentration dependent way. 1 ug/ml of sPLA 2 -IIA dramatically decreased the mRNA expression of eNOS. The protein expression of eNOS was not affected by sPLA 2 -IIA. (2) 4-BPB abolished the over expression of mRNA and protein of ICAM-1, VCAM-1 and ET-1 induced by the sPLA 2 -IIA. 4-BPB also abolished the up- regulated mRNA of eNOS and reduced the down-regulation of NO induced by sPLA 2 -IIA. (3) PD98059 abolished the over expression of ICAM-1, VCAM-1 and ET-1 and reduced the down-regulation of NO induced by the sPLA 2 -IIA. (4) SP600125 abolished the over expression of ET-1 and reduced the down-regulation of NO induced by sPLA 2 -IIA. (5) SB203580 had little effect on the over expression of ICAM-1, VCAM-1 and ET-1 and down-regulation of NO induced by sPLA 2 -IIA. 6. Bay11-7085 abolished the over expression of ICAM-1, VCAM-1 and ET-1 induced by the sPLA 2 -IIA. Conclusions (1) sPLA 2 -IIA induced the over expression of cytokines including ICAM-1, VCAM-1 and ET-1 in a concentration dependent manner or the repression of eNOS and NO. (2) Hydrolysis of sPLA 2 -IIA exactly take a part to regulate the expression of ICAM-1, VCAM-1, ET-1 and eNOS in endothelial cells. (3) sPLA 2 -IIA affect endothelial cells adhesion function primarily via ERK1/2 and NF-kB pathway. (4) sPLA 2 -IIA affect endothelial cells vasomotor function primarily via ERK1/2, JNK and NF-kB pathway.